The induction of cleft palates in A/J mice in response to the administration of a glucocorticoid offers an unusual laboratory model for studies on birth defects. Our hypothesis is that the genome is involved, and experiments are proposed to assay for various aspects of the genomic structure and function. The methods call for the fractionation of chromatin and assigning a well defined function to the various fractions. The latter is based on the assay for the presence of specific gene sequences in that fraction. These studies do not only include tissues from A/J mice but also tissues from other systems, such as from chicken and human placenta, to confirm the validity of assigning a specific function to a particular chromatin fraction. Our objectives include studies on the distribution of labeled triamcinolone acetonide in chromatin to look for the various binding sites for the labeled hormone both in active and inactive genes. Also we have isolated a fraction of chromosomal proteins which appears to be both gene and cell specific. We are attempting to find out whether there is a linkage in binding the hormone to chromatin and this fraction of chromosomal proteins. Such data will aid in understanding as to how clefting may occur in A/J mice in response to the exposure to teratogens, and may also aid in the final analysis as to how teratogens may influence development of the human embryo.